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    Alomone Labs ttx
    Effects of veratridine on human sperm motility in the presence of tetrodotoxin, <t>A-803467</t> or ab-66743. The effects of veratridine (10 μM) after different incubation times were analyzed in the presence of (A) the VGSC inhibitor tetrodotoxin <t>(TTX)</t> (10 nM) (B) TTX (10 μM), (C) the selective Na v 1.8 antagonist A-803467 (10 μM), (D) the Na v 1.8 antibody ab-66743 (dilution 1:50) or the corresponding solvent. Bars are means with SEM of 6-8 different experiments and represent percentage changes in progressive motility (grade A+B sperm) relative to the value observed at the same time in the respective solvent-treated paired controls. * P
    Ttx, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 96/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ttx/product/Alomone Labs
    Average 96 stars, based on 15 article reviews
    Price from $9.99 to $1999.99
    ttx - by Bioz Stars, 2022-08
    96/100 stars

    Images

    1) Product Images from "The Voltage-Gated Sodium Channel Nav1.8 Is Expressed in Human Sperm"

    Article Title: The Voltage-Gated Sodium Channel Nav1.8 Is Expressed in Human Sperm

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0076084

    Effects of veratridine on human sperm motility in the presence of tetrodotoxin, A-803467 or ab-66743. The effects of veratridine (10 μM) after different incubation times were analyzed in the presence of (A) the VGSC inhibitor tetrodotoxin (TTX) (10 nM) (B) TTX (10 μM), (C) the selective Na v 1.8 antagonist A-803467 (10 μM), (D) the Na v 1.8 antibody ab-66743 (dilution 1:50) or the corresponding solvent. Bars are means with SEM of 6-8 different experiments and represent percentage changes in progressive motility (grade A+B sperm) relative to the value observed at the same time in the respective solvent-treated paired controls. * P
    Figure Legend Snippet: Effects of veratridine on human sperm motility in the presence of tetrodotoxin, A-803467 or ab-66743. The effects of veratridine (10 μM) after different incubation times were analyzed in the presence of (A) the VGSC inhibitor tetrodotoxin (TTX) (10 nM) (B) TTX (10 μM), (C) the selective Na v 1.8 antagonist A-803467 (10 μM), (D) the Na v 1.8 antibody ab-66743 (dilution 1:50) or the corresponding solvent. Bars are means with SEM of 6-8 different experiments and represent percentage changes in progressive motility (grade A+B sperm) relative to the value observed at the same time in the respective solvent-treated paired controls. * P

    Techniques Used: Incubation

    2) Product Images from "Neuroepithelial progenitors generate and propagate non-neuronal action potentials across the spinal cord"

    Article Title: Neuroepithelial progenitors generate and propagate non-neuronal action potentials across the spinal cord

    Journal: bioRxiv

    doi: 10.1101/2020.05.23.111955

    Floor-plate biphasic action potentials are triggered by the activation of nicotinic acetylcholine receptors in response to acetylcholine released by motoneurons. a, Example of recurrent spontaneous floor-plate action potentials blocked after addition of the nicotinic acetylcholine receptor (nAChR) antagonists: Mecamylamine (50 μM) and d-Tubocurarine (5 μM). b, Example of current-clamp recording showing floor-plate action potential evoked by electrical stimulation in control condition (black trace) and after addition of the nAChR antagonists (red trace). c, Example of current-clamp recording showing floor-plate action potential evoked in control condition (black trace) and after addition of antagonists against ionotropic receptor for GABA (Gabazine 3 μM) and glutamate (DL-APV 200 μM and CNQX 20 μM). d, Example of current-clamp recording showing that floor-plate action potential can be evoked by local application of 30 μM acetylcholine (left trace), even in the presence of TTX (1 μM) and antagonists to AMPA/Kainate glutamate receptor (CNQX 10 μM), NMDA glutamate receptor (DL-APV 200 μM), GABA A receptor (Gabazine 3 μM) and glycine receptor (strychnine 1 μM) (center trace). Floor-plate action potential evoked by acetylcholine were blocked by the addition of nAChR antagonists (right trace). Note that the addition of TTX inhibited the fast component of the biphasic action potential (see Supplementary Figure 2 ). e, Confocal image of a coronal section from a ChAT:ChR2-YFP mouse embryo at E12.5 showing the expression of Channelrhodopsin2-YFP fusion protein (in green) in cholinergic motoneurons located in the ventro-dorsal horns and labelled with the vesicular acetylcholine transporter vAChT (in red). All cell nuclei were labelled using DAPI (in blue). f, Example of current-clamp recording from a ChAT:ChR2-YFP + motoneuron showing an action potential triggered by the opening of Channelrhodopsin 2 in response to blue light stimulation (470 nm). g, Example of current-clamp recording from a floor-plate cell recorded in a ChAT:ChR2-YFP + fetal spinal cord showing how blue light stimulation could evoke a slow cholinergic depolarization and trigger a biphasic action potential that were blocked by the addition of nAChR antagonists.
    Figure Legend Snippet: Floor-plate biphasic action potentials are triggered by the activation of nicotinic acetylcholine receptors in response to acetylcholine released by motoneurons. a, Example of recurrent spontaneous floor-plate action potentials blocked after addition of the nicotinic acetylcholine receptor (nAChR) antagonists: Mecamylamine (50 μM) and d-Tubocurarine (5 μM). b, Example of current-clamp recording showing floor-plate action potential evoked by electrical stimulation in control condition (black trace) and after addition of the nAChR antagonists (red trace). c, Example of current-clamp recording showing floor-plate action potential evoked in control condition (black trace) and after addition of antagonists against ionotropic receptor for GABA (Gabazine 3 μM) and glutamate (DL-APV 200 μM and CNQX 20 μM). d, Example of current-clamp recording showing that floor-plate action potential can be evoked by local application of 30 μM acetylcholine (left trace), even in the presence of TTX (1 μM) and antagonists to AMPA/Kainate glutamate receptor (CNQX 10 μM), NMDA glutamate receptor (DL-APV 200 μM), GABA A receptor (Gabazine 3 μM) and glycine receptor (strychnine 1 μM) (center trace). Floor-plate action potential evoked by acetylcholine were blocked by the addition of nAChR antagonists (right trace). Note that the addition of TTX inhibited the fast component of the biphasic action potential (see Supplementary Figure 2 ). e, Confocal image of a coronal section from a ChAT:ChR2-YFP mouse embryo at E12.5 showing the expression of Channelrhodopsin2-YFP fusion protein (in green) in cholinergic motoneurons located in the ventro-dorsal horns and labelled with the vesicular acetylcholine transporter vAChT (in red). All cell nuclei were labelled using DAPI (in blue). f, Example of current-clamp recording from a ChAT:ChR2-YFP + motoneuron showing an action potential triggered by the opening of Channelrhodopsin 2 in response to blue light stimulation (470 nm). g, Example of current-clamp recording from a floor-plate cell recorded in a ChAT:ChR2-YFP + fetal spinal cord showing how blue light stimulation could evoke a slow cholinergic depolarization and trigger a biphasic action potential that were blocked by the addition of nAChR antagonists.

    Techniques Used: Activation Assay, Expressing

    3) Product Images from "Corticotropin-releasing factor increases Purkinje neuron excitability by modulating sodium, potassium, and Ih currents"

    Article Title: Corticotropin-releasing factor increases Purkinje neuron excitability by modulating sodium, potassium, and Ih currents

    Journal: Journal of Neurophysiology

    doi: 10.1152/jn.00745.2015

    CRF elicits voltage changes in PN. A : the average of 4 responses of PN to local application of CRF (8 μM, red bar) at four different holding potentials in the presence of tetrodotoxin (TTX). Note the reversal of the response between −40 mV and −50 mV. B : ZD-7288 blocks the TTX-insensitive depolarizing response. The integral of the depolarizing response measured from CRF onset over a duration of 5.5 s under control conditions ( n = 21), in the presence of TTX ( n = 13) and TTX + ZD-7288 ( n = 15) is shown. C , first trace: whole cell recording of the average response to CRF application in the presence of TTX. Second trace: 8 pulses of −40 pA for 0.5 s, delivered at 1 Hz during CRF response. The third trace is the subtraction of the first trace from the second trace. Red bar denote the CRF application. Note the reduction in the response to current injections during CRF application. Fourth trace is the current injection protocol. D : the average reduction in input resistance during CRF application in 5 PN. E : a representative example of seven superimposed traces of the hyperpolarizing response of PN to CRF applications obtained from different holding potentials (−75 to −35 mV) and aligned by the membrane voltage before the application. F : the result shown in E plotted as a function of the membrane potential (red curve) and similar curves measured from another 5 cells (black curves). 2 μM CRF was used in C – F .
    Figure Legend Snippet: CRF elicits voltage changes in PN. A : the average of 4 responses of PN to local application of CRF (8 μM, red bar) at four different holding potentials in the presence of tetrodotoxin (TTX). Note the reversal of the response between −40 mV and −50 mV. B : ZD-7288 blocks the TTX-insensitive depolarizing response. The integral of the depolarizing response measured from CRF onset over a duration of 5.5 s under control conditions ( n = 21), in the presence of TTX ( n = 13) and TTX + ZD-7288 ( n = 15) is shown. C , first trace: whole cell recording of the average response to CRF application in the presence of TTX. Second trace: 8 pulses of −40 pA for 0.5 s, delivered at 1 Hz during CRF response. The third trace is the subtraction of the first trace from the second trace. Red bar denote the CRF application. Note the reduction in the response to current injections during CRF application. Fourth trace is the current injection protocol. D : the average reduction in input resistance during CRF application in 5 PN. E : a representative example of seven superimposed traces of the hyperpolarizing response of PN to CRF applications obtained from different holding potentials (−75 to −35 mV) and aligned by the membrane voltage before the application. F : the result shown in E plotted as a function of the membrane potential (red curve) and similar curves measured from another 5 cells (black curves). 2 μM CRF was used in C – F .

    Techniques Used: Injection

    4) Product Images from "Regional and Developmental Differences in Na+ Currents in Vestibular Primary Afferent Neurons"

    Article Title: Regional and Developmental Differences in Na+ Currents in Vestibular Primary Afferent Neurons

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2018.00423

    A TTX-insensitive current is present in immature calyces. (A) Control I Na and currents remaining in the presence of 200 nM TTX at membrane potentials above –60 mV in a P8 calyx (note different current scales for left and right panels). Voltage protocol similar to Figure 2 : a 40 ms step to –130 mV from a holding potential of –80 mV was followed by a series of 40 ms depolarizing steps in 10 mV increments from –90 to +20 mV. (B) Control (black) and response to 200 nM TTX (red) for nine calyces (P5–11) are shown in the IV plot of peak inward currents for steps between –80 and 0 mV. (C) Left panel: the residual current following 200 nM TTX is blocked in 1 μM TTX and the block reverses with washout in a P6 calyx. Currents in response to a voltage step from –130 to –30 mV. Right panel: 1 μM JZTX-III blocks a component of I Na and the remaining current is abolished following application of 1 μM JZTX-III plus 200 nM TTX in a P7 calyx. Currents in response to a voltage step from –130 to –50 mV. (D) Summary for a group of 12 cells perfused with 200 nM TTX (six cells at P5–6, six at P8–11). A group of cells exposed to 1 μM TTX ( n = 8, one cell at P6, seven cells at P7–10) I Na was abolished in 1 μM JZTX-III and 200 nM TTX ( n = 4, two cells at P6 and two cells at P7). Peak inward current was measured at –50 mV step. I Na tended to be larger at younger ages as shown by distributions. In the presence of 200 nM TTX, I Na decreased from –3.9 (1.8) to –0.25 (0.5) nA ( P
    Figure Legend Snippet: A TTX-insensitive current is present in immature calyces. (A) Control I Na and currents remaining in the presence of 200 nM TTX at membrane potentials above –60 mV in a P8 calyx (note different current scales for left and right panels). Voltage protocol similar to Figure 2 : a 40 ms step to –130 mV from a holding potential of –80 mV was followed by a series of 40 ms depolarizing steps in 10 mV increments from –90 to +20 mV. (B) Control (black) and response to 200 nM TTX (red) for nine calyces (P5–11) are shown in the IV plot of peak inward currents for steps between –80 and 0 mV. (C) Left panel: the residual current following 200 nM TTX is blocked in 1 μM TTX and the block reverses with washout in a P6 calyx. Currents in response to a voltage step from –130 to –30 mV. Right panel: 1 μM JZTX-III blocks a component of I Na and the remaining current is abolished following application of 1 μM JZTX-III plus 200 nM TTX in a P7 calyx. Currents in response to a voltage step from –130 to –50 mV. (D) Summary for a group of 12 cells perfused with 200 nM TTX (six cells at P5–6, six at P8–11). A group of cells exposed to 1 μM TTX ( n = 8, one cell at P6, seven cells at P7–10) I Na was abolished in 1 μM JZTX-III and 200 nM TTX ( n = 4, two cells at P6 and two cells at P7). Peak inward current was measured at –50 mV step. I Na tended to be larger at younger ages as shown by distributions. In the presence of 200 nM TTX, I Na decreased from –3.9 (1.8) to –0.25 (0.5) nA ( P

    Techniques Used: Blocking Assay

    5) Product Images from "The floor-plate of His is a non-neuronal electrical conduction pathway"

    Article Title: The floor-plate of His is a non-neuronal electrical conduction pathway

    Journal: bioRxiv

    doi: 10.1101/2020.05.23.111955

    Floor plate biphasic action potentials are triggered by the activation of nicotinic acetylcholine receptors in response to acetylcholine released by motoneurons. a , Example of recurrent spontaneous floor plate action potentials blocked after addition of the nicotinic acetylcholine receptor (nAChR) antagonists: Mecamylamine (50 µM) and d-Tubocurarine (5 µM). b , Example of current-clamp recording showing floor plate action potential evoked by electrical stimulation in control condition (black trace) and after addition of the nAChR antagonists (red trace). c , Example of current-clamp recording showing floor plate action potential evoked in control condition (black trace) and after addition of antagonists against ionotropic receptor for GABA (Gabazine 3 µM) and glutamate (DL-APV 200 µM and CNQX 20 µM). d , Example of current-clamp recording showing that floor plate action potential can be evoked by local application of 30 µM acetylcholine (left trace), even in the presence of TTX (1 µM) and antagonists to AMPA/Kainate glutamate receptor (CNQX 10 µM), NMDA glutamate receptor (DL-APV 200 µM), GABA A receptor (Gabazine 3 µM) and glycine receptor (strychnine 1 µM) (center trace). Floor plate action potential evoked by acetylcholine were blocked by the addition of nAChR antagonists (right trace). Note that the addition of TTX inhibited the fast component of the biphasic action potential (see Extended Data Figure 2 ). e , Confocal image of a coronal section from a ChAT:ChR2-YFP mouse embryo at E12.5 showing the expression of Channelrhodopsin2-YFP fusion protein (in green) in cholinergic motoneurons located in the ventro-dorsal horns and labelled with the vesicular acetylcholine transporter VAChT (in red). All cell nuclei were labelled using DAPI (in blue). f , Example of current-clamp recording from a ChAT:ChR2-YFP + motoneuron showing an action potential triggered by the opening of Channelrhodopsin 2 in response to blue light stimulation (470 nm). g , Example of current-clamp recording from a floor plate cell recorded in a ChAT:ChR2-YFP + fetal spinal cord showing how blue light stimulation could evoke a slow cholinergic depolarization and trigger a biphasic action potential that were blocked by the addition of nAChR antagonists.
    Figure Legend Snippet: Floor plate biphasic action potentials are triggered by the activation of nicotinic acetylcholine receptors in response to acetylcholine released by motoneurons. a , Example of recurrent spontaneous floor plate action potentials blocked after addition of the nicotinic acetylcholine receptor (nAChR) antagonists: Mecamylamine (50 µM) and d-Tubocurarine (5 µM). b , Example of current-clamp recording showing floor plate action potential evoked by electrical stimulation in control condition (black trace) and after addition of the nAChR antagonists (red trace). c , Example of current-clamp recording showing floor plate action potential evoked in control condition (black trace) and after addition of antagonists against ionotropic receptor for GABA (Gabazine 3 µM) and glutamate (DL-APV 200 µM and CNQX 20 µM). d , Example of current-clamp recording showing that floor plate action potential can be evoked by local application of 30 µM acetylcholine (left trace), even in the presence of TTX (1 µM) and antagonists to AMPA/Kainate glutamate receptor (CNQX 10 µM), NMDA glutamate receptor (DL-APV 200 µM), GABA A receptor (Gabazine 3 µM) and glycine receptor (strychnine 1 µM) (center trace). Floor plate action potential evoked by acetylcholine were blocked by the addition of nAChR antagonists (right trace). Note that the addition of TTX inhibited the fast component of the biphasic action potential (see Extended Data Figure 2 ). e , Confocal image of a coronal section from a ChAT:ChR2-YFP mouse embryo at E12.5 showing the expression of Channelrhodopsin2-YFP fusion protein (in green) in cholinergic motoneurons located in the ventro-dorsal horns and labelled with the vesicular acetylcholine transporter VAChT (in red). All cell nuclei were labelled using DAPI (in blue). f , Example of current-clamp recording from a ChAT:ChR2-YFP + motoneuron showing an action potential triggered by the opening of Channelrhodopsin 2 in response to blue light stimulation (470 nm). g , Example of current-clamp recording from a floor plate cell recorded in a ChAT:ChR2-YFP + fetal spinal cord showing how blue light stimulation could evoke a slow cholinergic depolarization and trigger a biphasic action potential that were blocked by the addition of nAChR antagonists.

    Techniques Used: Activation Assay, Expressing

    6) Product Images from "Impaired neural pathway in gastric muscles of patients with diabetes"

    Article Title: Impaired neural pathway in gastric muscles of patients with diabetes

    Journal: Scientific Reports

    doi: 10.1038/s41598-018-24147-y

    Electrical field stimulation (EFS)-induced response of distal gastric circular muscle strips after serial administration of atropine, MRS2500, N-nitro-L-arginine (L-NNA), and tetrodotoxin (TTX). ( a and b ) Atropine decreased the peak and TTX decreased the peak further in both the control subjects and diabetic patients. ( c ) MRS2500 increased the nadir but L-NNA abolished relaxation in the control subjects. ( d ) Also in the diabetic patients, L-NNA abolished relaxation. The Wilcoxon signed-rank test was used to evaluate the effects of each drug by compare values to the previous one.
    Figure Legend Snippet: Electrical field stimulation (EFS)-induced response of distal gastric circular muscle strips after serial administration of atropine, MRS2500, N-nitro-L-arginine (L-NNA), and tetrodotoxin (TTX). ( a and b ) Atropine decreased the peak and TTX decreased the peak further in both the control subjects and diabetic patients. ( c ) MRS2500 increased the nadir but L-NNA abolished relaxation in the control subjects. ( d ) Also in the diabetic patients, L-NNA abolished relaxation. The Wilcoxon signed-rank test was used to evaluate the effects of each drug by compare values to the previous one.

    Techniques Used:

    7) Product Images from "Selective Regulation of GluA Subunit Synthesis and AMPA Receptor-Mediated Synaptic Function and Plasticity by the Translation Repressor 4E-BP2 in Hippocampal Pyramidal Cells"

    Article Title: Selective Regulation of GluA Subunit Synthesis and AMPA Receptor-Mediated Synaptic Function and Plasticity by the Translation Repressor 4E-BP2 in Hippocampal Pyramidal Cells

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.3264-12.2013

    Facilitation of AMPAR-mediated unitary excitatory synaptic transmission in 4E-BP2 −/− mice. A , Increased spontaneous miniature synaptic activity in 4E-BP2 −/− mice. Top: Continuous 1 s recordings (in TTX, AP-5, and gabazine), showing more frequent and larger amplitude mEPSCs in pyramidal cells of 4E-BP2 −/− mice. Bottom: Summary bar graphs for all cells, showing a greater mEPSC amplitude and frequency in slices from 4E-BP2 −/− mice. B , Representative EPSCs evoked by minimal stimulation in pyramidal neurons illustrating larger responses in slices from 4E-BP2 −/− mice. Left: Superimposed 20 successive traces (EPSC successes + failures; gray) and mean response of 100 events (including failures; black). Middle: Mean EPSC pairs evoked by paired-pulse stimulation (50 ms interpulse interval), showing similar paired-pulse facilitation in 4E-BP2 −/− mice. The first and second EPSCs are superimposed on the right. Right: Superimposed scaled EPSC pairs showing that paired-pulse ratio is unchanged in slices from 4E-BP2 −/− mice. C , Summary bar graphs showing facilitation of EPSC potency (mean EPSC without failures) and similar failure rate and paired-pulse ratio in 4E-BP2 −/− mice. Data are mean ± SEM. * p
    Figure Legend Snippet: Facilitation of AMPAR-mediated unitary excitatory synaptic transmission in 4E-BP2 −/− mice. A , Increased spontaneous miniature synaptic activity in 4E-BP2 −/− mice. Top: Continuous 1 s recordings (in TTX, AP-5, and gabazine), showing more frequent and larger amplitude mEPSCs in pyramidal cells of 4E-BP2 −/− mice. Bottom: Summary bar graphs for all cells, showing a greater mEPSC amplitude and frequency in slices from 4E-BP2 −/− mice. B , Representative EPSCs evoked by minimal stimulation in pyramidal neurons illustrating larger responses in slices from 4E-BP2 −/− mice. Left: Superimposed 20 successive traces (EPSC successes + failures; gray) and mean response of 100 events (including failures; black). Middle: Mean EPSC pairs evoked by paired-pulse stimulation (50 ms interpulse interval), showing similar paired-pulse facilitation in 4E-BP2 −/− mice. The first and second EPSCs are superimposed on the right. Right: Superimposed scaled EPSC pairs showing that paired-pulse ratio is unchanged in slices from 4E-BP2 −/− mice. C , Summary bar graphs showing facilitation of EPSC potency (mean EPSC without failures) and similar failure rate and paired-pulse ratio in 4E-BP2 −/− mice. Data are mean ± SEM. * p

    Techniques Used: Transmission Assay, Mouse Assay, Activity Assay, Mass Spectrometry

    8) Product Images from "Dynamics of GnRH Neuron Ionotropic GABA and Glutamate Synaptic Receptors Are Unchanged during Estrogen Positive and Negative Feedback in Female Mice"

    Article Title: Dynamics of GnRH Neuron Ionotropic GABA and Glutamate Synaptic Receptors Are Unchanged during Estrogen Positive and Negative Feedback in Female Mice

    Journal: eNeuro

    doi: 10.1523/ENEURO.0259-17.2017

    Miniature GABA A receptor PSCs (mGPSCs) recorded from GnRH neurons do not change in the different mouse models of estrogen negative and positive feedback. A - F , Representative examples of mGPSC current recordings in the presence of AP5 (50 μM), CNQX (10 μM), and TTX (0.5 μM) taken from diestrous, OVX, OVX + E, and OVX + E+E mice. Underneath each trace an enlarged time scale of one mGPSC (*) is shown. C , F , mGPSCs are abolished by GABAzine (5 μM). G , H , Cumulative plots of the average inter-mGPSC interval ( G ) and amplitude ( H ) in the different experimental groups (for clarity only positive SEM is shown). N = 7 for each group. Cell numbers are shown in parenthesis. Numbers of PSCs analyzed is given in Table 1 . No statistically significant differences were detected for any parameter between groups.
    Figure Legend Snippet: Miniature GABA A receptor PSCs (mGPSCs) recorded from GnRH neurons do not change in the different mouse models of estrogen negative and positive feedback. A - F , Representative examples of mGPSC current recordings in the presence of AP5 (50 μM), CNQX (10 μM), and TTX (0.5 μM) taken from diestrous, OVX, OVX + E, and OVX + E+E mice. Underneath each trace an enlarged time scale of one mGPSC (*) is shown. C , F , mGPSCs are abolished by GABAzine (5 μM). G , H , Cumulative plots of the average inter-mGPSC interval ( G ) and amplitude ( H ) in the different experimental groups (for clarity only positive SEM is shown). N = 7 for each group. Cell numbers are shown in parenthesis. Numbers of PSCs analyzed is given in Table 1 . No statistically significant differences were detected for any parameter between groups.

    Techniques Used: Mouse Assay

    Miniature excitatory glutamate receptor PSCs (mEPSCs) recorded from GnRH neurons do not change in the different mouse models of estrogen negative and positive feedback. A - F , Representative examples of mEPSCs current recordings in the presence of GABAzine (5 μM) and TTX (0.5 μM) taken from diestrous, OVX, OVX + E, and OVX + E+E mice. Underneath each trace an enlarged time scale of one mEPSC (*) is shown. C , F , mEPSCs are abolished by AP5 (50 μM) + CNQX (10 μM). G , H , Cumulative plots of the average inter-mEPSC interval ( G ) and amplitude ( H ) in the different experimental groups (for clarity only positive SEM is shown). N = 5 for each group. Cell numbers are shown in parenthesis. Numbers of PSCs analyzed is given in Table 2 . No statistically significant differences were detected for any parameter between groups.
    Figure Legend Snippet: Miniature excitatory glutamate receptor PSCs (mEPSCs) recorded from GnRH neurons do not change in the different mouse models of estrogen negative and positive feedback. A - F , Representative examples of mEPSCs current recordings in the presence of GABAzine (5 μM) and TTX (0.5 μM) taken from diestrous, OVX, OVX + E, and OVX + E+E mice. Underneath each trace an enlarged time scale of one mEPSC (*) is shown. C , F , mEPSCs are abolished by AP5 (50 μM) + CNQX (10 μM). G , H , Cumulative plots of the average inter-mEPSC interval ( G ) and amplitude ( H ) in the different experimental groups (for clarity only positive SEM is shown). N = 5 for each group. Cell numbers are shown in parenthesis. Numbers of PSCs analyzed is given in Table 2 . No statistically significant differences were detected for any parameter between groups.

    Techniques Used: Mouse Assay

    9) Product Images from "Subunit- and pathway-specific localization of NMDA receptors and scaffolding proteins at ganglion cell synapses in rat retina"

    Article Title: Subunit- and pathway-specific localization of NMDA receptors and scaffolding proteins at ganglion cell synapses in rat retina

    Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience

    doi: 10.1523/JNEUROSCI.5602-08.2009

    Distinct NMDAR subtype contributions to sEPSCs at ON and OFF synapses. A, Average sEPSCs recorded form a morphologically identified ON RGC (V hold = −80 mV, 1 μM TTX, 100 μM D-serine, 0 [Mg 2+ ] o , inhibition blocked). Reducing glutamate uptake with the transporter antagonist TBOA (10 μM, green, 95 events averaged) conferred a slow component onto the sEPSC waveform compared to control (black, 135 events). This TBOA-induced component was reduced by the NR2B NMDAR-specific antagonist Ro-25,6981 (Ro, 1 μM, red, 106 events) and abolished completely by the pan-NMDAR antagonist CPP (10 μM, blue, 110 events). B , Summarized effects of TBOA, Ro-25,6981 and CPP in 5 ON RGCs. C , Average sEPSCs recorded from an identified OFF RGC in the same control conditions as above (black, 425 events). In the absence of TBOA, Ro-25,6981 (red, 202 events) had no effect on the sEPSC waveform but CPP blocked a slow component (blue, 88 events), indicating the presence of synaptic NMDARs that lack NR2B subunits. D , Summarized effects of Ro-25,6981 and CPP in 5 OFF RGCs. E , Average sEPSCs recorded from an identified OFF RGC in the same control conditions as above (black, 133 events). Addition of TBOA enhanced the sEPSC waveform (green, 110 events), revealing a component that was eliminated by Ro-25,6981 (red, 120 events). CPP reduced the sEPSC waveform further (blue, 100 events). F , Summarized effects of TBOA, Ro-25,6981 and CPP in 5 OFF RGCs. G , Average sEPSCs recorded from an identified OFF RGC in the presence of TBOA (with inhibition blocked), in control (2.5 mM) [Ca 2+ ] o (black, 89 events) or low (0.5 mM) [Ca 2+ ] o (gray, 59 events). H , Effects of changing [Ca 2+ ] o on sEPSC frequency and charge transfer in 4 OFF RGCs.
    Figure Legend Snippet: Distinct NMDAR subtype contributions to sEPSCs at ON and OFF synapses. A, Average sEPSCs recorded form a morphologically identified ON RGC (V hold = −80 mV, 1 μM TTX, 100 μM D-serine, 0 [Mg 2+ ] o , inhibition blocked). Reducing glutamate uptake with the transporter antagonist TBOA (10 μM, green, 95 events averaged) conferred a slow component onto the sEPSC waveform compared to control (black, 135 events). This TBOA-induced component was reduced by the NR2B NMDAR-specific antagonist Ro-25,6981 (Ro, 1 μM, red, 106 events) and abolished completely by the pan-NMDAR antagonist CPP (10 μM, blue, 110 events). B , Summarized effects of TBOA, Ro-25,6981 and CPP in 5 ON RGCs. C , Average sEPSCs recorded from an identified OFF RGC in the same control conditions as above (black, 425 events). In the absence of TBOA, Ro-25,6981 (red, 202 events) had no effect on the sEPSC waveform but CPP blocked a slow component (blue, 88 events), indicating the presence of synaptic NMDARs that lack NR2B subunits. D , Summarized effects of Ro-25,6981 and CPP in 5 OFF RGCs. E , Average sEPSCs recorded from an identified OFF RGC in the same control conditions as above (black, 133 events). Addition of TBOA enhanced the sEPSC waveform (green, 110 events), revealing a component that was eliminated by Ro-25,6981 (red, 120 events). CPP reduced the sEPSC waveform further (blue, 100 events). F , Summarized effects of TBOA, Ro-25,6981 and CPP in 5 OFF RGCs. G , Average sEPSCs recorded from an identified OFF RGC in the presence of TBOA (with inhibition blocked), in control (2.5 mM) [Ca 2+ ] o (black, 89 events) or low (0.5 mM) [Ca 2+ ] o (gray, 59 events). H , Effects of changing [Ca 2+ ] o on sEPSC frequency and charge transfer in 4 OFF RGCs.

    Techniques Used: Inhibition, Conditioned Place Preference

    10) Product Images from "Impaired neural pathway in gastric muscles of patients with diabetes"

    Article Title: Impaired neural pathway in gastric muscles of patients with diabetes

    Journal: Scientific Reports

    doi: 10.1038/s41598-018-24147-y

    Electrical field stimulation (EFS)-induced response of distal gastric circular muscle strips after serial administration of atropine, MRS2500, N-nitro-L-arginine (L-NNA), and tetrodotoxin (TTX). ( a and b ) Atropine decreased the peak and TTX decreased the peak further in both the control subjects and diabetic patients. ( c ) MRS2500 increased the nadir but L-NNA abolished relaxation in the control subjects. ( d ) Also in the diabetic patients, L-NNA abolished relaxation. The Wilcoxon signed-rank test was used to evaluate the effects of each drug by compare values to the previous one.
    Figure Legend Snippet: Electrical field stimulation (EFS)-induced response of distal gastric circular muscle strips after serial administration of atropine, MRS2500, N-nitro-L-arginine (L-NNA), and tetrodotoxin (TTX). ( a and b ) Atropine decreased the peak and TTX decreased the peak further in both the control subjects and diabetic patients. ( c ) MRS2500 increased the nadir but L-NNA abolished relaxation in the control subjects. ( d ) Also in the diabetic patients, L-NNA abolished relaxation. The Wilcoxon signed-rank test was used to evaluate the effects of each drug by compare values to the previous one.

    Techniques Used:

    11) Product Images from "TRPM8 Channel Activation Reduces the Spontaneous Contractions in Human Distal Colon"

    Article Title: TRPM8 Channel Activation Reduces the Spontaneous Contractions in Human Distal Colon

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms21155403

    Concentration–response curves for the inhibitory effects induced by DIPA 1–8 (1 nM–100 μM) before and after TTX (1 μM) ( A ) and TEA (10 mM) ( B ). All values are means ± S.E.M ( n = 6) and are expressed as percentage of inhibition of the spontaneous contractions. * p
    Figure Legend Snippet: Concentration–response curves for the inhibitory effects induced by DIPA 1–8 (1 nM–100 μM) before and after TTX (1 μM) ( A ) and TEA (10 mM) ( B ). All values are means ± S.E.M ( n = 6) and are expressed as percentage of inhibition of the spontaneous contractions. * p

    Techniques Used: Concentration Assay, Inhibition

    12) Product Images from "Subunit- and pathway-specific localization of NMDA receptors and scaffolding proteins at ganglion cell synapses in rat retina"

    Article Title: Subunit- and pathway-specific localization of NMDA receptors and scaffolding proteins at ganglion cell synapses in rat retina

    Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience

    doi: 10.1523/JNEUROSCI.5602-08.2009

    Distinct NMDAR subtype contributions to sEPSCs at ON and OFF synapses. A, Average sEPSCs recorded form a morphologically identified ON RGC (V hold = −80 mV, 1 μM TTX, 100 μM D-serine, 0 [Mg 2+ ] o , inhibition blocked). Reducing glutamate uptake with the transporter antagonist TBOA (10 μM, green, 95 events averaged) conferred a slow component onto the sEPSC waveform compared to control (black, 135 events). This TBOA-induced component was reduced by the NR2B NMDAR-specific antagonist Ro-25,6981 (Ro, 1 μM, red, 106 events) and abolished completely by the pan-NMDAR antagonist CPP (10 μM, blue, 110 events). B , Summarized effects of TBOA, Ro-25,6981 and CPP in 5 ON RGCs. C , Average sEPSCs recorded from an identified OFF RGC in the same control conditions as above (black, 425 events). In the absence of TBOA, Ro-25,6981 (red, 202 events) had no effect on the sEPSC waveform but CPP blocked a slow component (blue, 88 events), indicating the presence of synaptic NMDARs that lack NR2B subunits. D , Summarized effects of Ro-25,6981 and CPP in 5 OFF RGCs. E , Average sEPSCs recorded from an identified OFF RGC in the same control conditions as above (black, 133 events). Addition of TBOA enhanced the sEPSC waveform (green, 110 events), revealing a component that was eliminated by Ro-25,6981 (red, 120 events). CPP reduced the sEPSC waveform further (blue, 100 events). F , Summarized effects of TBOA, Ro-25,6981 and CPP in 5 OFF RGCs. G , Average sEPSCs recorded from an identified OFF RGC in the presence of TBOA (with inhibition blocked), in control (2.5 mM) [Ca 2+ ] o (black, 89 events) or low (0.5 mM) [Ca 2+ ] o (gray, 59 events). H , Effects of changing [Ca 2+ ] o on sEPSC frequency and charge transfer in 4 OFF RGCs.
    Figure Legend Snippet: Distinct NMDAR subtype contributions to sEPSCs at ON and OFF synapses. A, Average sEPSCs recorded form a morphologically identified ON RGC (V hold = −80 mV, 1 μM TTX, 100 μM D-serine, 0 [Mg 2+ ] o , inhibition blocked). Reducing glutamate uptake with the transporter antagonist TBOA (10 μM, green, 95 events averaged) conferred a slow component onto the sEPSC waveform compared to control (black, 135 events). This TBOA-induced component was reduced by the NR2B NMDAR-specific antagonist Ro-25,6981 (Ro, 1 μM, red, 106 events) and abolished completely by the pan-NMDAR antagonist CPP (10 μM, blue, 110 events). B , Summarized effects of TBOA, Ro-25,6981 and CPP in 5 ON RGCs. C , Average sEPSCs recorded from an identified OFF RGC in the same control conditions as above (black, 425 events). In the absence of TBOA, Ro-25,6981 (red, 202 events) had no effect on the sEPSC waveform but CPP blocked a slow component (blue, 88 events), indicating the presence of synaptic NMDARs that lack NR2B subunits. D , Summarized effects of Ro-25,6981 and CPP in 5 OFF RGCs. E , Average sEPSCs recorded from an identified OFF RGC in the same control conditions as above (black, 133 events). Addition of TBOA enhanced the sEPSC waveform (green, 110 events), revealing a component that was eliminated by Ro-25,6981 (red, 120 events). CPP reduced the sEPSC waveform further (blue, 100 events). F , Summarized effects of TBOA, Ro-25,6981 and CPP in 5 OFF RGCs. G , Average sEPSCs recorded from an identified OFF RGC in the presence of TBOA (with inhibition blocked), in control (2.5 mM) [Ca 2+ ] o (black, 89 events) or low (0.5 mM) [Ca 2+ ] o (gray, 59 events). H , Effects of changing [Ca 2+ ] o on sEPSC frequency and charge transfer in 4 OFF RGCs.

    Techniques Used: Inhibition

    13) Product Images from "Nitrergic Pathway Is the Major Mechanism for the Effect of DA-9701 on the Rat Gastric Fundus Relaxation"

    Article Title: Nitrergic Pathway Is the Major Mechanism for the Effect of DA-9701 on the Rat Gastric Fundus Relaxation

    Journal: Journal of Neurogastroenterology and Motility

    doi: 10.5056/jnm13098

    Electrical field stimulation-induced response of the rat gastric fundus longitudinal muscle strips after serial administration of atropine, DA-9701, N-nitro-L-arginine (L-NNA), MRS2500 and tetrodotoxin (TTX). (A, B) When atropine was added, peak and nadir did not show significant change (by Wilcoxon signed ranks test). (C, D) When DA-9701 (0.5, 5, 25 and 50 μg) was added in the presence of atropine, peak and nadir did not show significant dose-dependent change (Kruskal Wallis test for testing differences in EFS-induced contractile responses for different DA-9701 doses). (E) Subsequent addition of L-NNA, MRS2500 and TTX in the presence of atropine and DA-9701 (50 μg) did not affect peak (compared with previous value by Wilcoxon signed ranks test). (F) Subsequent addition of L-NNA in the presence of atropine and DA-9701 (50 μg) decreased nadir by inhibiting relaxation, while addition of MRS2500 and TTX in the presence of atropine, DA-9701 (50 μg) and L-NNA did not affect nadir further ( * P
    Figure Legend Snippet: Electrical field stimulation-induced response of the rat gastric fundus longitudinal muscle strips after serial administration of atropine, DA-9701, N-nitro-L-arginine (L-NNA), MRS2500 and tetrodotoxin (TTX). (A, B) When atropine was added, peak and nadir did not show significant change (by Wilcoxon signed ranks test). (C, D) When DA-9701 (0.5, 5, 25 and 50 μg) was added in the presence of atropine, peak and nadir did not show significant dose-dependent change (Kruskal Wallis test for testing differences in EFS-induced contractile responses for different DA-9701 doses). (E) Subsequent addition of L-NNA, MRS2500 and TTX in the presence of atropine and DA-9701 (50 μg) did not affect peak (compared with previous value by Wilcoxon signed ranks test). (F) Subsequent addition of L-NNA in the presence of atropine and DA-9701 (50 μg) decreased nadir by inhibiting relaxation, while addition of MRS2500 and TTX in the presence of atropine, DA-9701 (50 μg) and L-NNA did not affect nadir further ( * P

    Techniques Used:

    14) Product Images from "Human Breast Cancer Cells Demonstrate Electrical Excitability"

    Article Title: Human Breast Cancer Cells Demonstrate Electrical Excitability

    Journal: Frontiers in Neuroscience

    doi: 10.3389/fnins.2020.00404

    VGSC activity of MDA-MB-231 cells. VGSC activity was blocked using TTX (20 μM). (A) Current trace showing electrical activity before, during and after application of TTX. (B) Quantification of the spikes recorded in (A) . Number of spikes were measured in time bins of 6 min. Bars represent average values of all 3 repeats and error bars represent SDs.
    Figure Legend Snippet: VGSC activity of MDA-MB-231 cells. VGSC activity was blocked using TTX (20 μM). (A) Current trace showing electrical activity before, during and after application of TTX. (B) Quantification of the spikes recorded in (A) . Number of spikes were measured in time bins of 6 min. Bars represent average values of all 3 repeats and error bars represent SDs.

    Techniques Used: Activity Assay, Multiple Displacement Amplification

    15) Product Images from "Regional and Developmental Differences in Na+ Currents in Vestibular Primary Afferent Neurons"

    Article Title: Regional and Developmental Differences in Na+ Currents in Vestibular Primary Afferent Neurons

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2018.00423

    A TTX-insensitive current is present in immature calyces. (A) Control I Na and currents remaining in the presence of 200 nM TTX at membrane potentials above –60 mV in a P8 calyx (note different current scales for left and right panels). Voltage protocol similar to Figure 2 : a 40 ms step to –130 mV from a holding potential of –80 mV was followed by a series of 40 ms depolarizing steps in 10 mV increments from –90 to +20 mV. (B) Control (black) and response to 200 nM TTX (red) for nine calyces (P5–11) are shown in the IV plot of peak inward currents for steps between –80 and 0 mV. (C) Left panel: the residual current following 200 nM TTX is blocked in 1 μM TTX and the block reverses with washout in a P6 calyx. Currents in response to a voltage step from –130 to –30 mV. Right panel: 1 μM JZTX-III blocks a component of I Na and the remaining current is abolished following application of 1 μM JZTX-III plus 200 nM TTX in a P7 calyx. Currents in response to a voltage step from –130 to –50 mV. (D) Summary for a group of 12 cells perfused with 200 nM TTX (six cells at P5–6, six at P8–11). A group of cells exposed to 1 μM TTX ( n = 8, one cell at P6, seven cells at P7–10) I Na was abolished in 1 μM JZTX-III and 200 nM TTX ( n = 4, two cells at P6 and two cells at P7). Peak inward current was measured at –50 mV step. I Na tended to be larger at younger ages as shown by distributions. In the presence of 200 nM TTX, I Na decreased from –3.9 (1.8) to –0.25 (0.5) nA ( P
    Figure Legend Snippet: A TTX-insensitive current is present in immature calyces. (A) Control I Na and currents remaining in the presence of 200 nM TTX at membrane potentials above –60 mV in a P8 calyx (note different current scales for left and right panels). Voltage protocol similar to Figure 2 : a 40 ms step to –130 mV from a holding potential of –80 mV was followed by a series of 40 ms depolarizing steps in 10 mV increments from –90 to +20 mV. (B) Control (black) and response to 200 nM TTX (red) for nine calyces (P5–11) are shown in the IV plot of peak inward currents for steps between –80 and 0 mV. (C) Left panel: the residual current following 200 nM TTX is blocked in 1 μM TTX and the block reverses with washout in a P6 calyx. Currents in response to a voltage step from –130 to –30 mV. Right panel: 1 μM JZTX-III blocks a component of I Na and the remaining current is abolished following application of 1 μM JZTX-III plus 200 nM TTX in a P7 calyx. Currents in response to a voltage step from –130 to –50 mV. (D) Summary for a group of 12 cells perfused with 200 nM TTX (six cells at P5–6, six at P8–11). A group of cells exposed to 1 μM TTX ( n = 8, one cell at P6, seven cells at P7–10) I Na was abolished in 1 μM JZTX-III and 200 nM TTX ( n = 4, two cells at P6 and two cells at P7). Peak inward current was measured at –50 mV step. I Na tended to be larger at younger ages as shown by distributions. In the presence of 200 nM TTX, I Na decreased from –3.9 (1.8) to –0.25 (0.5) nA ( P

    Techniques Used: Mass Spectrometry, Blocking Assay

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    Effects of veratridine on human sperm motility in the presence of tetrodotoxin, <t>A-803467</t> or ab-66743. The effects of veratridine (10 μM) after different incubation times were analyzed in the presence of (A) the VGSC inhibitor tetrodotoxin <t>(TTX)</t> (10 nM) (B) TTX (10 μM), (C) the selective Na v 1.8 antagonist A-803467 (10 μM), (D) the Na v 1.8 antibody ab-66743 (dilution 1:50) or the corresponding solvent. Bars are means with SEM of 6-8 different experiments and represent percentage changes in progressive motility (grade A+B sperm) relative to the value observed at the same time in the respective solvent-treated paired controls. * P
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    Effects of veratridine on human sperm motility in the presence of tetrodotoxin, A-803467 or ab-66743. The effects of veratridine (10 μM) after different incubation times were analyzed in the presence of (A) the VGSC inhibitor tetrodotoxin (TTX) (10 nM) (B) TTX (10 μM), (C) the selective Na v 1.8 antagonist A-803467 (10 μM), (D) the Na v 1.8 antibody ab-66743 (dilution 1:50) or the corresponding solvent. Bars are means with SEM of 6-8 different experiments and represent percentage changes in progressive motility (grade A+B sperm) relative to the value observed at the same time in the respective solvent-treated paired controls. * P

    Journal: PLoS ONE

    Article Title: The Voltage-Gated Sodium Channel Nav1.8 Is Expressed in Human Sperm

    doi: 10.1371/journal.pone.0076084

    Figure Lengend Snippet: Effects of veratridine on human sperm motility in the presence of tetrodotoxin, A-803467 or ab-66743. The effects of veratridine (10 μM) after different incubation times were analyzed in the presence of (A) the VGSC inhibitor tetrodotoxin (TTX) (10 nM) (B) TTX (10 μM), (C) the selective Na v 1.8 antagonist A-803467 (10 μM), (D) the Na v 1.8 antibody ab-66743 (dilution 1:50) or the corresponding solvent. Bars are means with SEM of 6-8 different experiments and represent percentage changes in progressive motility (grade A+B sperm) relative to the value observed at the same time in the respective solvent-treated paired controls. * P

    Article Snippet: In parallel experiments, the effect of veratridine or its solvent was investigated in aliquots pretreated during the last 15 min of capacitation with the specific Na v 1.8 antagonist A-803467 (Sigma) (1 μM) [ ] or during capacitation (2 h) with TTX (Alomone Labs, Jerusalem, Israel)) (0.01 or 10 μM), the Na v 1.8 antibody ab-66743 (dilution 1:50) or the corresponding solvent.

    Techniques: Incubation